Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient with seropositive rheumatoid arthritis and a carrier of hepatitis B surface antigen developed angiofollicular hyperplasia (multicentric Castleman's disease). The hepatitis B virus and the rheumatoid factor may have had a role in the aetiology of this lymphatic disorder. The development of Castleman's disease in association with these factors may provide another clue supporting the reactive nature of this disease.
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PMID:Multicentric Castleman's disease associated with rheumatoid arthritis: a possible role of hepatitis B antigen. 271 14

A simple and specific enzyme-linked immunosorbent assay (ELISA) has been developed to detect circulating IgG and IgM anti-idiotypic antibodies directed against anti-HBs molecules using 96-well polyvinyl microtitre plates as the solid phase and HRPO-labelled goat anti-HBs as conjugate. Anti-idiotype reactions were observed in the supernatant portion after precipitation of immune complexes from sera with polyethylene glycol 6000 (PEG). Both IgG and IgM with anti-idiotype activity were detected concurrently in HBsAg-positive sera from HBV-infected patients and asymptomatic HBV carriers. Anti-idiotype activity was absent in HBsAg-negative sera from healthy persons, and in patients with non-A, non-B hepatitis and viral hepatitis A. However, such antibodies could be demonstrated in the sera of two out of eight HBsAg vaccine recipients negative for anti-HBs but in none of 11 recipients positive for anti-HBs after receiving a booster immunising dose of HBsAg vaccine. Those sera showing positive anti-idiotype reactions were free from rheumatoid factor and HBsAg/IgM or HBsAg/IgG complex activity. An analysis of anti-idiotype positive sera for anti-HBs, HBeAg and HBV-specific DNA-polymerase activity demonstrated these markers in 20%, 30% and 60% of cases, respectively. The presence of anti-idiotypic antibodies was presumed to permit a more active multiplication of hepatitis B virus.
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PMID:An enzyme-linked immunosorbent assay (ELISA) for the detection of IgG and IgM anti-idiotypes directed against anti-HBs molecules. 294 20

Vasculitis is a syndrome which may complicate certain infectious, rheumatic, and allergic diseases. We identified 13 patients, over the past 17 years, who had both vasculitis and lympho- or myeloproliferative disorders and relate their clinical, laboratory, histologic, and immunologic features, course, therapy, and outcome. Nine patients were male, 4 female; ages ranged from 28 to 82 years. Ten of 13 patients presented with cutaneous vasculitis antedating malignancy by an average of 10 months. Three of 13 developed cutaneous vasculitis after malignancy. A statistically significant association between cutaneous vasculitis and lympho- or myeloproliferative malignancies was noted when compared with all other tumors. Dermatologic manifestations included palpable purpura (5 patients), maculopapular eruptions (4), urticarial and petechial lesions (3), and ulcers (1). Hepatitis B surface antigen, Coombs antibodies, rheumatoid factor and antinuclear antibodies were not found. Serum cryoglobulins were detected in 3 patients; serum C3 and C4 were normal in 8 of 9 patients evaluated. Histologic examinations revealed necrotizing leukocytoclastic vasculitis with disruption of endothelial integrity, destruction of endothelium, and neutrophil infiltration. Occasional perivascular mononuclear cell invasion was also noted in 4 patients. Immunofluorescent staining for IgG, IgA, IgM, C3, and C4 was negative in all patients studied. Symptoms were, in general, poorly responsive to therapy, which included nonsteroidal antiinflammatory drugs, antihistamines, antiserotonin agents, and corticosteroids. Chemotherapy directed at the underlying malignancy was also generally ineffective, although the vasculitis appeared to lessen in severity. Vasculitis appeared to lessen in severity as bone marrow function deteriorated. Ten patients died, all as a direct result of their malignancy. We have described a unique clinical syndrome of lympho- and myeloproliferative disease presenting with small-vessel vasculitis. Recognition that rheumatic symptoms may reflect or antedate malignancy may permit early diagnosis, aggressive treatment, and elucidation of pathogenesis.
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PMID:Vasculitis associated with malignancy. Experience with 13 patients and literature review. 329 73

The clinical and laboratory data regarding the presence of serum markers of hepatitis B virus (HBV) were studied in a group of patients with necrotizing vasculitis. A high incidence of skin and articular alterations, of cryoglobulinemia and rheumatoid factor, was observed in HBsAg carriers. The potential role of HBV in the pathogenesis of systemic vasculitis is discussed.
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PMID:Observations on HBsAg positive systemic vasculitis. 342 1

There is a need for a simple, sensitive, specific, and inexpensive test for immunoglobulin M antibody to hepatitis B core antigen (anti-HBc IgM). A solid phase passive hemagglutination test (SP-PHA) was developed for this purpose and compared with the enzyme-linked immunosorbent assay (ELISA) test. Hepatitis B core antigen (HBcAg) used in PHA and SP-PHA was synthesized in Escherichia coli. Human IgM was captured to a microtiter plate coated with anti-human IgM, and the presence of anti-HBc IgM was demonstrated by the adherence of HBcAg-sensitized erythrocytes to the bottom of a U-shaped microtiter plate. ELISA and SP-PHA were made at 1:100 and 1:1,000 serum dilution, respectively. Both were positive in 100% of 36 cases of acute hepatitis B, 68.18% of 22 cases of chronic hepatitis B, and 20% of 75 healthy carriers of hepatitis B surface antigen (HBsAg) but none in 65 anti-HBc-positive blood donors that had negative results for HBsAg. Results of both tests were identical but were false positive because rheumatoid factor was found only in ELISA. End-point titration by SP-PHA and PHA was also found useful for the differentiation of acute hepatitis B from chronic hepatitis B and HBsAg carriers.
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PMID:A new solid phase passive hemagglutination test for IgM antibody to hepatitis B core antigen. 381 60

An IgM-specific anti-[anti-HBs] antibody was detected by radioimmunoassay using anti-IgM-coated beads and 125I-labeled anti-HBs. This antiidiotype was found only in the sera of hepatitis B virus-infected patients, both acute and chronic. However, not all HBsAg-positive patients exhibited this reaction, and activity was correlated with the presence of HBeAg. Approximately 93% of sera that contained antiidiotype activity also contained HBeAg. Conversely, 70% of the sera positive for HBeAg reacted in the IgM assay. No correlation was observed between the presence of antiidiotype and rheumatoid factor or elevated SGPT levels. Two approaches were used to determine whether the reactive moiety was an IgM anti-[anti-HBs] as postulated or an IgM anti-HBs/HBsAg complex. It was shown that chicken anti-HBs sera, which does not share the common idiotype of human and other mammalian anti-HBs, did not block a positive reaction in this radioimmunoassay even though it specifically bound HBsAg. It was also demonstrated that treatment with polyethylene glycol, which will precipitate IgM anti-HBs/HBsAg activity, did not precipitate the reactive moiety in 6 of 7 sera tested, lending further evidence to the existence of an IgM antiidiotype in these patients. It is suggested that this antiidiotype directed against anti-HBs may be involved in a defective feedback mechanism resulting in the suppression of production of anti-HBs and maintenance of the carrier state.
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PMID:Detection of an IgM antiidiotype directed against anti-HBs in hepatitis B patients. 387 43

A new capture enzyme immunoassay for the determination of immunoglobulin M (IgM) antibodies against hepatitis B core antigen (HBcAg) is described. Core antigen produced in Escherichia coli was labeled with biotin and subsequently detected by an avidin-biotin-peroxidase complex. The biotin-labeled core antigen was effective at concentrations as low as 20 ng/ml. Of 561 serum samples from different groups of patients that were tested, 465 samples were negative for other hepatitis B virus markers and also for anti-HBcAg IgM. Sera from the early stages of hepatitis B infection had high levels of anti-HBcAg IgM, and a clear correlation with the acuteness of the disease was observed in 45 follow-up sera from 23 patients with acute or recent hepatitis B. Sera from 21 patients with past hepatitis B were all negative for anti-HBcAg IgM. Twenty serum samples from chronic carriers of hepatitis B surface antigen showed slightly elevated antibody levels for anti-HBcAg IgM. Ten sera which were positive for anti-HBcAg IgG antibodies and had high levels of rheumatoid factor were negative for anti-HBcAg IgM.
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PMID:Determination of immunoglobulin M antibodies for hepatitis B core antigen with a capture enzyme immunoassay and biotin-labeled core antigen produced in Escherichia coli. 390 76

The evaluation of an enzyme-linked immunosorbent assay (ELISA) test designed to detect antigens of hepatitis non A, non B (HNANB) revealed that a rheumatoid factor (RF)-like reaction was interfering. This RF-like reaction was not detectable by routine screening methods for RF, such as latex agglutination or the Waaler Rose test. Testing of sequential sera of chimpanzees with acute HNANB showed that this RF-like reaction was present in the acute phase of HNANB simultaneously with alanine aminotransferase (ALT) elevations. Characterization of this RF-like reaction revealed the presence of an IgM antibody against human IgG that banded in CsCl at 1.3 g/ml and at 19S in sucrose gradients. Absorption with IgG-coated latex particles and anti-human IgM gave further evidence of an RF. By testing sera of patients with different forms of acute viral hepatitis, it was demonstrated that an RF-like factor was also present in seven sera from 9 patients with acute hepatitis A, in two sera from 11 patients with hepatitis B, and seven sera from 11 patients with acute HNANB. The rise of RF in the acute phase of hepatitis A may be an effect of polyclonal stimulation of IgM producing B lymphocytes. The high prevalence of RF in HNANB remains unclear as no polyclonal stimulation of IgM has been observed.
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PMID:Demonstration of a transient rheumatoid factor in the acute phase of hepatitis non A, non B. 392 Mar 53

A sandwich ELISA for hepatitis B virus surface antigen (HBsAg) was developed using monoclonal anti-HBs for the solid phase and horse-radish peroxidase labelled sheep anti-HBs. The sensitivity was approx. 0.3 U/ml HBsAg, in the standard test procedure, comprising two incubation steps of 1 h at 37 degrees C, or in a shortened procedure comprising two incubation steps of 30 min at 50 degrees C. A slightly reduced sensitivity (approx. 0.5 U/ml) was obtained when the two incubations were combined in a one-step incubation for 1 h at 37 degrees C. All three procedures were completed by an incubation for 30 min at room temperature with peroxide and tetra-methylbenzidine. The number of false positives obtained when donor sera were screened was below 0.5%. False positive reactions occurred more frequently, but still to a limited extent, when previously selected sera containing rheumatoid factor or other possibly interfering factors were tested with the standard procedure. Most sera containing factors that interfere with a commercial ELISA for HBsAg using sheep anti-HBs coated plates, were negative. Rheumatoid factor positive sera seldom gave false positive results. The lower detection limit became approx. 0.1 U/ml when the cut-off was reduced, while the number of false positives in a donor population only increased to 1.5%. The results obtained with reagents from four different batches indicate a stability of up to 4 wk at 37 degrees C and for at least 26 wk at 4 degrees C.
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PMID:Improved ELISA for the detection of HBsAg. 399 41

Ninety-four sera from 23 patients with necrotizing vasculitis of the polyarteritis nodosa (PAN) type were examined for immune complexes by polyethylene glycol (PEG) precipitation. The presence of immune complexes in serum specimens was positively correlated with the presence of active disease in PAN (p less than .001). These complexes predicted active disease 93% of the time and their absence predicted a period of inactivity 54% of the time. The presence of hepatitis B markers, Clq immune complexes, rheumatoid factor, or low complement levels did not correlate with active disease. In 9 patients in whom serial specimens were tested for immune complexes there was a positive association of immune complexes and active PAN.
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PMID:Correlation of disease activity in systemic necrotizing vasculitis with immune complexes. 611 70


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